Evidence map›Paper›PMID 22331845›Full record

ArticleThe Journal of cell biology2012

A neuropeptide signaling pathway regulates synaptic growth in Drosophila.

Xu Chen, Barry Ganetzky

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.2field-weighted citation impact, top 12% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

35 citing papers in PubMed, 68 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. The neuropeptide drosulfakinin enhances choosiness and protects males from the aging effects of social perception.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Identification of sulfakinin receptors (SKR) in Tenebrio molitor beetle and the influence of sulfakinins on carbohydrates metabolism.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2020
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Xu ChenLaboratory of Genetics, University of Wisconsin-Madison, Madison, WI 53706, USA.
Barry Ganetzky
University of Wisconsin–Madison · US

Funding

Neurogenetics of TS-Paralytic Mutants in DrosophilaR01NS015390 · NINDS · UNIVERSITY OF WISCONSIN-MADISON · PI GANETZKY, BARRY S · 1985 to 2011
$4.5M
NINDS NIH HHS NS15390NINDS NIH HHS R01 NS015390
6 · The paper itself

Abstract

Neuropeptide signaling is integral to many aspects of neural communication, particularly modulation of membrane excitability and synaptic transmission. However, neuropeptides have not been clearly implicated in synaptic growth and development. Here, we demonstrate that cholecystokinin-like receptor (CCKLR) and drosulfakinin (DSK), its predicted ligand, are strong positive growth regulators of the Drosophila melanogaster larval neuromuscular junction (NMJ). Mutations of CCKLR or dsk produced severe NMJ undergrowth, whereas overexpression of CCKLR caused overgrowth. Presynaptic expression of CCKLR was necessary and sufficient for regulating NMJ growth. CCKLR and dsk mutants also reduced synaptic function in parallel with decreased NMJ size. Analysis of double mutants revealed that DSK/CCKLR regulation of NMJ growth occurs through the cyclic adenosine monophosphate (cAMP)-protein kinase A (PKA)-cAMP response element binding protein (CREB) pathway. Our results demonstrate a novel role for neuropeptide signaling in synaptic development. Moreover, because the cAMP-PKA-CREB pathway is required for structural synaptic plasticity in learning and memory, DSK/CCKLR signaling may also contribute to these mechanisms.

Indexed as

Signal TransductionAnimalsAnimals, Genetically ModifiedCloning, MolecularCyclic AMPCyclic AMP-Dependent Protein KinasesCyclic AMP Response Element-Binding ProteinDrosophila melanogasterDrosophila ProteinsElectrophysiologyFemaleImmunoenzyme TechniquesLarvaMaleMutationNeuromuscular JunctionCCKLR-17D3 protein, DrosophilaCyclic AMPCyclic AMP-Dependent Protein KinasesCyclic AMP Response Element-Binding ProteinDrosophila Proteinsdrosulfakinin 1NeuropeptidesOligopeptidesReceptors, Cholecystokinin

Identifiers

PMID22331845
PMCPMC3283997
OpenAlexW2107297721

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.